Differential gene expression between individuals exposed to different levels of air pollution
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE7543 | GEO | 2008/04/17
SECONDARY ACCESSION(S): PRJNA99375
REPOSITORIES: GEO
Similar Datasets
Project description:Comparison of genome-wide gene expression between humans living in areas of high levels of air pollution and less polluted areas. Experiment Overall Design: The study investigated differential gene expression in peripheral blood from 23 children and 12 adults from a region of residence with high levels of air pollution as compared to 24 children and 12 adults from a less-polluted area.Two conditions: living in the polluted or in the less-polluted area. One individual per array, hybridized against a common reference sample
2008-06-15 | E-GEOD-7543 | biostudies-arrayexpress
Project description:Air pollutants including particulate matter (PM) and chemicals adsorbed onto PM pose a serious threat to human health. In this study, we analyzed the ability of PM to induce diverse gene expression profile modulation after chronic exposure in subjects living in two regions of the Czech Republic differing in levels and sources of the air pollution. We also considered impact of different seasonal conditions on concentrations and compositions of PM. Blood samples of 312 subjects from polluted Ostrava city and 154 controls from Prague city were collected in winter 2009, summer 2009 and winter 2010. The highest concentrations of air pollutants were detected in winter 2010 when the subjects were exposed to: PM of aerodynamic diameter < 2.5 M-BM-5m (70 vs. 44.9 M-BM-5g/m3); benzo[a]pyrene (9.02 vs. 2.56 ng/m3) and benzene (10.2 vs. 5.5 M-BM-5g/m3) in Ostrava and Prague, respectively. Global gene expression analysis of total RNA extracted from leukocytes was performed using whole genome microarrays (Illumina). The expression of selected genes was verified by quantitative real-time PCR (qRT-PCR). Despite lower concentrations of air pollutants we found a higher number of differentially expressed genes and affected KEGG pathways in subjects from Prague. In both locations we observed differences between seasons. The qRT-PCR analysis showed a significant decrease in expression of APEX, ATM, FAS, GSTM1, IL1B and RAD21 in subjects from Ostrava, in a comparison of winter 2010 and summer 2009. In Prague, an increase in gene expression was observed for GADD45A and PTGS2. In conclusion, high concentrations of pollutants in Ostrava do not increase the number of differentially expressed genes. This may be explained by adaption of humans to chronic exposure to air pollution. Total RNA was extracted from leukocytes of total of 154 control subjects and 312 subjects exposed to heavy air pollution. The samples were collected in three seasons (winter 2009, summer 2009, winter 2010) with different levels of air pollution. Most of the subjects were sampled repeatedly; however, some of them joined the study in summer 2009 or winter 2010.
2014-08-27 | E-GEOD-60767 | biostudies-arrayexpress
Project description:SINERGIA-Phyllosphere bacteria and air pollution
| PRJEB28871 | ENA
Project description:In the present study, we investigate pulmonary transcriptional responses in mice following exposure in situ to ambient air in a heavily polluted urban environment. Mature C57BL/CBA male mice were caged in sheds located in an urban area near two working steel mills and a major highway in Hamilton, Ontario, Canada. Control mice were housed in the same environment but received only high-efficiency particle-filtered air. Whole lung tissues were collected from mice exposed for 3 weeks, 10 weeks or for 10 weeks followed by 6 weeks in the laboratory (16 weeks total). DNA microarrays were used to explore changes in pulmonary gene expression in mice breathing ambient air versus HEPA-filtered air. Transcriptional profiling revealed changes in the expression of genes implicated in the lipid droplet synthesis pathway (plin, dgat2, lpl, s3-12, agpat2), antioxidants (ucp1). We postulate that exposure to particulate matter adsorbed with polycyclic aromatic hydrocarbons triggers lipid droplet synthesis (holding depots for lipids and malformed/excess proteins tagged for degradation) in the lungs, which act to sequester particulates adsorbed with toxic chemicals. Increased lipid droplet synthesis could potentially lead to endogenous/stressor-induced synthesis of reactive oxygen species and activation of antioxidant mechanisms. Further investigation into the stimulation of lipid droplet synthesis in the lung in response to air pollution is warranted in order to better understand these mechanistic changes and the resulting health implications.
2013-09-30 | GSE41698 | GEO
Project description:Rationale: DNA methylation plays a critical role in asthma development, but differences in DNA methylation associated with asthma severity, especially among adults, are less well-defined. Changes in DNA methylation are influenced by exposure to air pollution, which is a risk factor for asthma exacerbation and severity. Here, we examined how DNA methylomic patterns in adult asthmatics differ by asthma severity and exposure to different components of air pollution. Methods: Peripheral blood CD3+ T cells from adult asthmatics in Beijing, China were serially collected from 37 patients (130 samples total) and analyzed for global DNA methylation using the Illumina MethylationEPIC Array. Measurements and Main Results: Significant differences in DNA methylation were noted among subjects with different degrees of asthma severity, as measured by fraction of exhaled nitric oxide, forced expiratory volume, and asthma control test scores. Differences in DNA methylation were annotated to genes that were enriched in pathways related to asthma or T cell function, and included gene ontology categories related to cellular adhesion, developmental pathways, and calcium signaling. Notable genes that were differentially methylated based on asthma severity included RUNX3, several members of the HLA family, PDGFRA, CDH1, CAV1, and NOTCH4. Differences in DNA methylation also varied by exposure to ambient air pollution, with different components of pollution effecting methylation of different groups of genes. Conclusion: These findings demonstrate how adult asthmatics possess widespread differences in the DNA methylation that associated with varying asthma severity and how air pollution might contribute to more severe asthma via changes in DNA methylation.
2024-07-31 | GSE226257 | GEO
Project description:The study comprises of 24 subjects that have been exposed to high and low Traffic-related air pollution.
2022-01-01 | GSE125647 | GEO
Project description:To investigate the cellular responses induced by air pollution exposures, we performed genome-wide gene expression microarray analysis using whole blood RNA sampled at three time-points across the work weeks of 63 non-smoking employees in the trucking industry. Our objective was to identify the genes and gene networks differentially activated in response to micro-environmental measures of occupational exposure to three pollutants: PM2.5 (particulate matter ≤ 2.5 microns in diameter) and elemental carbon (EC) and organic carbon (OC).
2016-07-08 | GSE83864 | GEO
Project description:We analyzed the ability of particulate matter (PM) and chemicals adsorbed onto it to induce diverse gene expression profiles in subjects living in two regions of the Czech Republic differing in levels and sources of the air pollution. A total of 312 samples from polluted Ostrava region and 154 control samples from Prague were collected in winter 2009, summer 2009 and winter 2010. The highest concentrations of air pollutants were detected in winter 2010 when the subjects were exposed to: PM of aerodynamic diameter < 2.5 µm (PM2.5) (70 vs. 44.9 µg/m3); benzo[a]pyrene (9.02 vs. 2.56 ng/m3) and benzene (10.2 vs. 5.5 µg/m3) in Ostrava and Prague, respectively. Global gene expression analysis of total RNA extracted from leukocytes was performed using Illumina Expression BeadChips microarrays. The expression of selected genes was verified by quantitative real-time PCR (qRT-PCR). Gene expression profiles differed by locations and seasons. Despite lower concentrations of air pollutants a higher number of differentially expressed genes and affected KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways was found in subjects from Prague. In both locations immune response pathways were affected, in Prague also neurodegenerative diseases-related pathways. Over-representation of the latter pathways was associated with the exposure to PM2.5. The qRT-PCR analysis showed a significant decrease in expression of APEX, ATM, FAS, GSTM1, IL1B and RAD21 in subjects from Ostrava, in a comparison of winter 2010 and summer 2009. In Prague, an increase in gene expression was observed for GADD45A and PTGS2. In conclusion, high concentrations of pollutants in Ostrava were not associated with higher number of differentially expressed genes, affected KEGG pathways and expression levels of selected genes. This observation suggests that chronic exposure to air pollution may result in reduced gene expression response with possible negative health consequences.
2014-08-27 | GSE60767 | GEO
Project description:Atopic dermatitis is increasing worldwide, correlating with air pollutions. Various organic components of pollutants activate transcription factor AhR (aryl-hydrocarbon receptor). We have established AhR-CA mice, whose keratinocytes express constitutive-active AhR, and these mice developed atopic dermatitis-like frequent scratching and allergic inflammation. In this study we performed ChIP-seq analyses and identified keratinocyte-specific AhR target genes, including inflammatory cytokines Tslp and IL33, and neurotrophic factor Artemin. While AhR-CA mice exhibited epidermal hyperinnervation and alloknesis leading to hypersensitivity to pruritus, blockade of Artemin alleviated these phenotypes. AhR-CA mice showed scratching-induced barrier insufficiency and enhanced sensitization to epicutaneously-applied antigens, recapitulating human atopic dermatitis. Consistently, AhR activation and Artemin expression was detected in the epidermis of atopic dermatitis patients and keratinocytes exposed to air pollutants. Thus, AhR in keratinocytes senses the environmental stimuli and responds to them through moderating inflammation. We propose a mechanism in which air pollution induces atopic dermatitis through AhR activation.
2016-11-13 | GSE72449 | GEO
Project description:Empirical evidence from both animals and humans suggest that PM2.5 (particulate matter < 2.5μm) exposure accelerates a variety of non-communicable diseases (NCDs) including Type 2 diabetes. We investigated whether chronic exposure to ambient air pollution (PM2.5), disrupts circadian rhythm to facilitate metabolic insulin resistance and compared the impact of inhaled ambient PM2.5 alone or in combination with continuous light exposure (LL). Exposure to PM2.5 induced peripheral IR, disrupted circadian steroid release, reduced peak oxygen consumption and altered brown adipose 18Ffluorodeoxyglucose uptake on PET imaging. These findings were identical to that seen with LL with no additive interaction between PM2.5 and LL. Transcriptome profiles in the liver revealed a number of differentially expressed circadian genes Bmal1 (Arntl/Npas2), Period (Per) and Cryptochrome (Cry) in response to PM2.5. Alteration in chromatin accessibility in circadian targets was observed with PM2.5 by Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) while chromatin immunoprecipitation (ChIP) analysis, showed a marked difference in promoter occupancy by p300. Our data suggest a previously unrecognized role of particulate air pollution in promoting circadian disruption and metabolic dysfunction through epigenetic regulation of multiple circadian targets
2020-12-01 | GSE145566 | GEO